Maternal chelation for embryo, fetal and infant benefit

ABSTRACT

This invention teaches the use of chelating agents to diagnose and treat metal toxins in a patient. Chelation agents are given to the mother for the benefit of the baby. Metal toxins such as lead, arsenic, mercury, tin, antimony, aluminum and others are known to cause miscarriages, birth defects, maldevelopment of the organs and tissues and maldevelopment of the brain. Chelation treatments of the mother can prevent these problems in the embryo, fetus and infant. Removal of lead and mercury and other toxins allows improved development of the offspring, both during the chelation and after the chelation is discontinued. Determining whether a mother who has just delivered a baby has elevated levels of heavy metals can also be used to identify the elevated metals of the mother as a possible cause of birth defects.

CROSS-REFERENCE TO RELATED APPLICATIONS

This application claims priority to U.S. Utility application Ser. No.11/536,795, filed Sep. 29, 2006, which claims priority to and thebenefit of U.S. Provisional Patent Application No. 60/722,907, filedSep. 30, 2005. The entire disclosures of U.S. Utility application Ser.No. 11/536,795 and U.S. Provisional Patent Application No. 60/722,907are hereby incorporated herein by reference.

BACKGROUND OF THE INVENTION

1. Field of the Invention

This invention relates generally to the field of medicine, and moreparticularly to a method of enhancing the embryonic, fetal, conceptus,infant, and human child development by chelation treatment of the motherto remove toxic substances.

2. Related Art

There are a number of diagnostic methods, treatment regimens andpreventative measures that the medical community has encouraged andpatients have taken to reduce the occurrences of birth defects,miscarriages, infertility disorders and childhood neurologicdysfunctions. However, even with currently known therapies, there aretoo many birth defects, miscarriages, infertility disorders andchildhood neurologic dysfunctions. As societies moved away from theirorganic agricultural bases to industrialized manufacturing economies,including the use of chemical pesticides and industrial techniques forfarming, the environment in which people live has become less organicand more toxic. Therefore, while industrialized societies greatlyimprove health care, there are much greater environmental hazards facingpeople, particularly metal toxins that build up within a person'ssystem. To date, there has not been a comprehensive methodology todiagnose, isolate and remove these metal toxins. Instead, industrializedsocieties have sought solutions without regard to their environmentaltoxins.

Birth defects have, in the past, been prevented by the use of folate, bythe use of multivitamins, by abstaining from alcohol and harmful drugs,and by avoidance of carotenoids such as vitamin A. Avoidance ofcarotenotic drugs has also been done. However, birth defects are stilltoo common, with a prevalence of 2 to 4 percent (2%-4%) among live borninfants. Most birth defects, approximately 70%, have no known cause.

Miscarriages are also too common with 15% of pregnancies ending inmiscarriage, and in the vast majority of cases, no cause is found. Metaltoxins can cause birth defects, spontaneous abortion, and/ormiscarriage.

Miscarriage is common: as stated previously, approximately 15% of allpregnancies end in miscarriage. Miscarriages can be caused by uterineabnormalities which can be treated with uterine surgery. Miscarriagescan be caused by antiphospholipid antibody syndrome, and these have beentreated with heparin, aspirin and steroids. Miscarriages can be causedby thrombophilias in which an inherited abnormality of one of theproteins controlling the clotting cascade causes malfunction.Thrombophilias have been treated with anticoagulants such as aspirinand/or heparin. Miscarriage can be caused by diabetes, and treatment ofdiabetes has reduced the rate of miscarriage. This treatment includesinsulin for blood sugar control and metformin for insulin resistance.Miscarriages caused by hypothyroidism can be treated with thyroidreplacement.

While it is acknowledged that miscarriages are caused by lead, mercuryor other heavy metal toxins, no program has been advanced other than thelimited Foresight program. Foresight Great Britain has developed aprogram for the prevention of birth defects and miscarriage. Thisprogram identifies mineral toxicities by means of hair analysis. Metaltoxins, when found, are treated with vitamin C, nutrient minerals andmultivitamins, and selenium. However, the Foresight program issub-optimal because it is limited to using hair analysis rather than aprovocative chelation or even a blood analysis without a provocativechelation, and it is not expressly directed to quantifying and removingmetal toxins using chelation treatments. Accordingly, itsrecommendations are limited to supplementing the patient's diet withselenium and vitamin C, rather than selecting from a range of chelationtreatments that should be considered when toxic metals are identified,particularly including the use of more effective synthetic chelators.

Mental retardation affects approximately 3% of children, and somestudies indicate that attention deficit disorder may affect 20%-40% ofall children. Mild variants of minimal brain dysfunction, includingdisorders of auditory and/or visual perception and/or processing, aretoo common. Minor degrees of abnormal neurologic development can bemanifested by behavioral, developmental or other neurologicabnormalities. All told, there is an abundance of childhood neurologicdysfunction which leads to behavioral problems, emotional problems,intellectual problems, lost learning, reduced intelligence and decreasedintellectual capacity and job performance.

Diagnosis and treatment of childhood neurologic dysfunction has beenlargely postnatal and thus too late. Postnatal problems that causemental deficits include inborn errors of metabolism. These have beendiagnosed with urinary amino acids, urinary organic acids, and otherbiochemical tests postnatally. Chromosomal analysis has enabled thediagnosis of neurologic dysfunctions secondary to chromosomal disorders.Few, if any, treatments are known for chromosomal disorders. No anatomicmaldevelopment may be detected by imaging studies of the brain includingultrasound, MRI or CAT scan. Most of these conditions have no knowntreatment. Genetic syndromes can be identified as a cause of mentalretardation by examination and inspection of the affected child, thefacial and physical exam findings may suggest one or more geneticsyndromes that can be tested for either by DNA methods, by chromosomalmethods or by biochemical methods.

Lead poisoning is commonly investigated and detected postnatally by ablood test or occasionally by provocative challenge with a chelationagent. Chelation treatments have long been given to children to removelead. Chelation agents used on children for removal of lead include DMSAand EDTA. While it is known that lead can accumulate in fetusesantenatally, no program of fetal detoxification has been advocatedprenatally because synthetic chelating agents are thought to beteratogenic. However, other work has suggested that studies showingharmful effects of chelators might have been due to a failure in thosestudies to co-administer mineral supplements to the patient along withthe chelators. Thus in those studies the adverse outcomes observedfollowing chelation therapy might have been due to the chelators havingleached essential minerals from the patient's body rather than anyharmful effects of the chelating chemicals themselves. Nonetheless,chelators have only been given to mothers for severe maternal toxicitybut not for fetal benefit. No chelation treatment has ever been done formothers with lead, mercury, aluminum, or antimony levels that are belowwhat is considered acutely toxic.

Mercury is known to cause cerebral palsy and mental deficits. This wasshown from an outbreak of mercury toxicity that occurred in Japan whereit has caused Minamata disease. Another outbreak of mercury poisoningoccurred in Iraq. Mercury is widely thought to cause autism wheninjected with vaccinations. For this reason, the mercurial preservativethimerosol has been removed from most vaccinations. Additionally,mercury vapor, which may arise from amalgam dental fillings, is known tocross the placenta and affect the fetus. Other than the Foresightprogram, there is no program to identify and detoxify preconceptionalwomen, pregnant women, or lactating women so that toxins will notaccumulate in the baby and affect embryonic, fetal, neonatal or infantdevelopment. Additionally, there is no program to identify similartoxins in men and to detoxify these men with chelation therapies priorto impregnating their partners. The standard of care for improving fetaloutcome is prenatal diagnosis. In prenatal diagnosis, ultrasoundexaminations are done on fetuses. In some cases, chromosomal analysis isdone. When problems are detected, termination is offered to the mother.This system has limited effectiveness because: 1. many abnormalities aremissed, 2. mild abnormalities are missed, 3. abnormalities ofneurological function are usually missed, and 4. many mothers refusetermination when it is offered.

The problems with the above-discussed approach of testing women who arealready pregnant are as follows: 1) Prevention of mental deficit byprenatal diagnosis and selective abortion cannot be universally appliedand is harmful to the fetus: the resultant death to the fetus isobjectionable to many, and, therefore, is often refused; 2) Lead,mercury and almost all teratogens have their greatest effect early indevelopment when the embryo/fetus is most vulnerable and susceptible.Treatment early in the development would have a much more profoundbeneficial effect than treatment later in development.

There are half as many children in the United States today withintelligence quotients (IQs) above 130 than there were in pastgenerations. The effects of heavy metals, herbicides, pesticides, andorganic toxins on early brain development last for decades. Regions withhigher infant mortality also have higher rates of emphysema seventy (70)years later. The health of the gravid female during pregnancy makes forhealthy babies, adolescents, and adults. The removal of heavy metals bytherapeutic chelation of the pregnant woman will likely lead toincreased IQ's, increased scores on neurological development tests likethe Denver Developmental Exam, and higher scores on standardized testsof the offspring years after the treatment of the gravid female hasconcluded. Higher order mental and neurologic function include but arenot limited to those traits which are well known to lead to higherscores on IQ tests, standardized tests, neurologic ability tests andentrance exams for colleges and professional schools.

As discussed above, the Foresight program is insufficient in itsdiagnostic evaluation of the patient and in its treatment regimen. Whilethis program has some usefulness, it is too limited of a program fordiagnosing and treating symptomatic adults. Given the grave threat posedby metal toxins to the fetus, more aggressive treatment may result inenhancement of neurologic development and performance.

SUMMARY OF THE INVENTION

Reproductive chelation treatments can be given to the mother beforeconception, during pregnancy and/or during lactation forfetal/embryonic/neonatal benefit. The chelation therapy consists oftreating the mother with a chelating agent so as to benefit heroffspring. The goals are to remove metal toxins so as to prevent birthdefects, miscarriages, suboptimal organ development including braindevelopment and to enhance the neurologic development both during andafter pregnancy and lactation.

In one embodiment, the invention is a method of attenuating orpreventing human birth defects, spontaneous abortions, infertility andchildhood neurological dysfunctions caused by subclinical levels ofheavy metals including the steps of identifying the presence ofsubclinical levels of heavy metals in a fertile human female;calculating a suitable dosage of a synthetic chelating agent; andadministering the dosage of the synthetic chelating agent to thepregnant human female.

In another aspect, the invention is a method of attenuating orpreventing human birth defects, miscarriages, infertility and childhoodneurological dysfunctions caused by subclinical levels of heavy metalsin a pregnant human, including the steps of identifying the presence ofsubclinical levels of heavy metals in the pregnant human; calculating asuitable dosage of a proteinaceous chelating agent; and administeringthe dosage of the proteinaceous chelating agent to the pregnant human.

In still another aspect, the invention is a method of determining acause of a birth defect, miscarriage, infertility and childhoodneurological dysfunction including delivering an infant from a humanfemale; administering chelating agents to the human female; collecting aurine sample from the human female; and analyzing the urine sample forthe presence of heavy metals.

In yet another aspect, the invention is a method of reducing an amountof a heavy metal in a pregnant human including the steps of diagnosingthe presence of subclinical levels of the heavy metal in the pregnanthuman; calculating a suitable dosage of a synthetic chelating agent; andadministering the dosage of the synthetic chelating agent to thepregnant human.

Further areas of applicability of the present invention will becomeapparent from the detailed description provided hereinafter. Forexample, while the chelation therapies described herein are for mothers,it should be appreciated that chelation therapy may also be used todiagnose metal toxins in men and detoxify these men prior to theirimpregnation of their respective partners. It should be understood thatthe detailed description and specific examples, while indicating thepreferred embodiment of the invention, are intended for purposes ofillustration only and are not intended to limit the scope of theinvention.

DETAILED DESCRIPTION OF THE INVENTION

The invention contemplates various well known routes of administrationfor the chelating agents; these include intravenous bolus, intramuscularbolus, transdermal application and oral administration. DMPS would bemost preferably administered transdermally, orally, or intravenously(IV). DMSA would be administered transdermally, or orally. EDTA iscontemplated to be administered orally and intravenously. Penicillamineis contemplated to be administered orally. EDTA is contemplated to beadministered orally. Lactate is contemplated to be administeredintravenously. Proteinaceous chelators are contemplated to beadministered orally, transdermally or intravenously.

Metals contemplated by the invention as targets for chelation therapyinclude but are not limited to di- and trivalent metal cations, lead,mercury, cadmium, aluminum, cobalt, gallium, lithium, arsenic,beryllium, copper, manganese, nickel, and vanadium. The specificityprofiles for the various known chelating agents are well known by theskilled artisan.

The invention contemplates the use of well known chemical chelatingagents, both organic and inorganic, in fertile women, including pregnantwomen. Chemical chelating agents contemplated by this invention for usewith the disclosed methods include chelators of divalent and trivalentcations, including synthetic agents such as Ethylenediamine Tetra-aceticAcid (EDTA), British Anti-Lewisite (BAL), Dimercaptosuccinic Acid(DMSA), Dimercaptopropanesulfonic Acid (DMPS),Cyclohexanediaminetetraacetic Acid (CDTA),Diethylenetriaminepenta-acetic Acid (DTPA), Dipicolinic Acid &/orD-Penicillamine (DPA), N-Acetyl-Cysteine (NAC), Dihydroxy-benzeneDisulfonic Acid (TIRON), Deferoxamine (DFO), and Triethylenetetramine(TRIEN), as well as substances such as ampicillin, lactate,penicillamine, desferroxamine, Vitamin C, pyruvate, porphyrins, purines,pyrimidines, RNA, DNA, amino acids, and crown ethers.

Similarly, this invention contemplates the use of proteinaceouschelating agents. Examples of proteinaceous chelating agentscontemplated by this invention include transferrin, ferritin,metallothionine, albumin, heparin, and synthetically designed proteinsengineered for specific binding coefficients, metal specificity, andexcretability in the feces.

Chelation agents must be administered to the patient at the properdosage so as not to induce mineral deficiencies. EDTA should beadministered at a dosage of about 1.5 g-3 g per day or about 42 mg/kg ofmaternal body weight. DMSA should be administered at about 10 mg/kg/day.

EDTA is contemplated to be administered in dosages in the range of0.21-430 mg/kg/day, and more particularly in the range of 21-43mg/kg/day. DMSA is contemplated to be administered in dosages in therange of 0.1-100 mg/kg/day, and more particularly in the range of 5-15mg/kg/day and most particularly in a dosage of 10 mg/kg/day. One DMSAcycle is 3 days on, 11 days off. Alternatively, DMSA could beadministered at 5 to 10 day cycles if administered early in pregnancyDMPS is contemplated to be administered in dosages of 0.5-10 mg/kg, upto 2-3 days/week, assessing the urine samples after every fifth to tenthchallenge, or when reaching a decision point in therapy, i.e. attemptingto achieve pregnancy.

When chelating agents are used in a preconceptional female, they may beused either with family planning or without family planning. With familyplanning, they may be used from daily to biweekly. When chelating agentsare used in the female who is trying to achieve pregnancy, they areideally limited to a period of infertility at the beginning of thecycle. This period of infertility begins with the onset of heavy ormoderate bleeding, denoting a normal menstrual period. The period endswith the onset of fertile mucus, at approximately the 8^(th) to the11^(th) day of the menstrual cycle.

By a “fertile human female” what is meant is a woman who is capable ofconceiving children or who is pregnant.

The terms “diagnostic provocation” and “chelation-provoked urine tests”and related terms refer to a procedure whereby the patient isadministered one of more dosages of chelators, after which the patient'surine is collected for a defined period of time. The collected urine isanalyzed for metal content, the metal having been removed from thepatient's body by the chelators. The results of this procedure canindicate which metals are present in the patient's body and theapproximate levels of the metals, which is subsequently used indesigning a course of chelation therapy.

In addition to the above-mentioned ‘diagnostic provocation’ method ofdiagnosing the presence of metals in a patient's body, other suchdiagnostic methods include urinary analysis (without prior provocationwith chelators), blood testing, red blood cell analysis, and hairanalysis and use corresponding specimens.

Besides mercury and lead, other potentially toxic metals that may besusceptible to chelation treatment include cadmium, arsenic, aluminum,antimony, uranium, and thorium. In addition many of these metals canhave synergistic effects when more than one is present in the patient'sbody, such as the combination of mercury and lead.

The range of normal lab values for toxic metals is the subject of somedebate. The metals may be measured with or without prior chelationprovocation. The standard values accepted by medical laboratories aremeasured without chelation provocation. Treatment with chelationmedication mobilizes metal stores within in the body to be detected inthe urine, thus values obtained post-provocation will be increased. Thedifference between pre- and post-provocation is also of value in that itreveals the degree of metal toxin burden in the body. It should also benoted that all values used by medical laboratories refer to adultpatients. There is currently no level of metal toxins known to be safefor the developing fetus; i.e. the normal value is 0.00 mcg/g(micrograms/gram of creatinine).

Table I below lists a number of metal toxins with the accepted upperlimit of normal, acceptable levels (i.e. “subclinical” levels),expressed as micrograms per gram of creatinine (mcg/g) as measured in aurine sample. Subclinical levels of metals are those at or below whichimmediate medical attention is not considered to be necessary, i.e.there is not thought to be acute toxicity associated with these levelsor below, but above which immediate medical treatment including possiblechelation therapy may be undertaken.

TABLE I Aluminum 22 mcg/g Antimony 0.14 mcg/g Barium 7.88 mcg/g Bismuth0.76 mcg/g Boron 5.7 mcg/g Cadmium 0.64 mcg/g Cesium 10.5 mcg/gGadolinium 0.02 mcg/g Gallium 0.028 mcg/g Lead 1.4 mcg/g Mercury 2.14mcg/g Molybdenum 0.18 mcg/g Nickel 9.5 mcg/g Palladium controversialPlatinum 0.033 mcg/g Rubidium 2,263 mcg/g Selenium 0.35 mcg/g Thallium0.298 mcg/g Thorium 0.124 mcg/g Tin 2.04 mcg/g Tungsten 0.211 mcg/gUranium 0.026 mcg/g

Table II is similar to Table I, but it lists toxic elements involumetric concentrations as measured over a twenty-four (24) hourperiod (micrograms/24 hours, i.e., mcg/24 hr).

TABLE II Aluminum 25.2 mcg/24 hr Antimony 0.144 mcg/24 hr Arsenic 49mcg/24 hr Barium 5.5 mcg/24 hr Bismuth 0.70 mcg/24 hr Cadmium 0.63mcg/24 hr Cesium 10.1 mcg/24 hr Gadolinium 0.019 mcg/24 hr Gallium 0.031mcg/24 hr Lead 1.5 mcg/24 hr Mercury 2.17 mcg/24 hr Nickel 4.41 mcg/24hr Niobium 0.086 mcg/24 hr Platinum 0.038 mcg/24 hr Rubidium 2.486mcg/24 hr Thallium 0.273 mcg/24 hr Thorium 0.108 mcg/24 hr Tin 2.25mcg/24 hr Tungsten 0.264 mcg/24 hr Uranium 0.027 mcg/24 hr

Chelation therapy should proceed via the procedures outlined above untilthe metal levels are within the normal limits listed above. It will beappreciated that as the dangerous effects of these toxins are furtherrealized, the limits that are considered normal will be expected todecrease over time. For example, some of the actual examples discussedbelow were begun when the normal limit of mercury was more than twicethe limit listed above.

To avoid side effects that might arise from the chelators depletingessential minerals from the patient's body, chelators are generallyco-administered with mineral supplements, such as zinc.

PROPHETIC EXAMPLES Example 1 Chelation in the Gravid Female withSub-Clinically Materna-Toxic Levels of Lead, Mercury, Aluminum, orAntimony for the Benefit of the Conceptus

In this embodiment, a pregnant female would present to the health careworker to be diagnosed for the presence of sub clinically toxic levelsof metals. The mother would be given a provocative challenge test usingone or more well known chelating agents like for example EDTA. Assumingthe mother's levels of toxic metals were shown not to be acutelyhazardous to the mother and merely within the subclinical range such asshown in Table I, the pregnant female would then be a candidate formaternal chelation therapy. For example, if the level of a particularmetal as measured in the mother's urine is at or above the ‘acceptable’levels shown in Table I above, then the mother would be a candidate formaternal chelation therapy. The levels of a particular metal in amother's body that are considered to be ‘subclinical’ for the mothermight nonetheless be harmful for a developing fetus.

The weight of the mother would be determined. The weight of the motherwould then be used to determine the dosage of chelation agents using thedosage information provided hereinabove. The chelating agent would beprovided on alternating days with mineral supplementation. The dosage ofEDTA for a prototypical 70 kg pregnant female would be preferably in therange of 21-43 mg/kg/day. The chelation dosing would continue for aperiod of days to weeks. Another factor in calculating the chelatordosages may be based on the gestational age of the fetus. For example,in the first trimester, one half of the typical adult dosage could beused, while 70% of the typical adult dosage could be used in the secondtrimester, and 90% of the typical adult dosage could be used in thethird trimester. Once the levels of lead, mercury, aluminum or antimonyreached acceptable (preferably undetectable) levels, the chelationregimen would be altered from a detoxification regimen to a maintenanceregimen. This maintenance regimen would continue until birth and beyond.A maintenance regimen would consist of chelation therapy during thefirst 3-8 days of each menstrual cycle, continuing until pregnancy isachieved, using dosages as described above.

Example 2 Co-Administration of Chelating Agents with MineralSupplementation or Administration of Chelating Agents Bound to NormalMinerals to Forestall Birth Defects Due to Chelation Therapy

In this embodiment, a pregnant female would present to the health careworker to be diagnosed for the presence of sub clinically toxic levelsof metals. The mother would be given a provocative challenge test usingone or more well known chelating agents, for example EDTA. Assuming themother's levels of toxic metals were shown not to be acutely hazardousto the health of the mother, the pregnant female may still be acandidate for maternal chelation therapy for the benefit of the baby. Incomparison, prior art chelation treatments for pregnant females havebeen limited to those situations where the mother is so toxic that shemust be treated regardless of any concern for the baby.

DMSA would be co-administered with zinc to the gravid female. DMSA wouldthus bind or chelate zinc in the stomach and then be absorbed in theblood stream. Upon entering the gravid females system, the DMSA wouldexchange the bound zinc for toxic metals and would then be excreted.Because chelation therapy with DMSA alone might deplete zinc levels inthe absence of mineral supplementation, zinc deficiency and itsteratogenic effects would be avoided. The use of a chelating agent toenhance absorption of essential minerals on the way in, and thereby topick up and excrete heavy metal toxins on the way out, may be called“boomerang” chelation. Boomerang chelation could be performed asfollows. The chelating agent is administered orally with essentialminerals, especially these weakly bond by chelator. Since there will bea high concentration of weakly bond minerals in the stomach, these willbe absorbed due to mass action. Once absorbed, the chelator will findmore preferred cations, especially strongly bound metal toxins. In theurine, it will be bound in the toxins. By transporting nutrient mineralsin, the teratogenic effect of the chelator may be defeated.

The weight of the mother would be determined. The weight of the motherwould then be used to determine the dosage of chelation agent and themineral supplement to be co-administered using the dosage informationprovided hereinabove. The chelating agent would be provided onalternating days with mineral supplementation provided every day duringthe pregnancy.

The dosage of EDTA for a prototypical 70 kg pregnant female would bepreferably in the range of 21-43 mg/kg/day. The chelation dosing wouldcontinue for a period of days to weeks. Once the levels of lead,mercury, aluminum or antimony reached acceptable (preferablyundetectable) levels, the chelation regimen would be altered from adetoxification regiment to a maintenance regimen. This maintenanceregiment would continue until birth and beyond.

Example 3 Maternal Diagnostic Chelation of the Post-Partum Human Femaleand Neonate for the Purpose of Determining the Cause of Birth Defects,Still Birth, Miscarriage, Fetal Distress or Other NeurologicalImpairment

A child is born with one or more birth defects. The parents would liketo know the cause. A foley catheter is inserted into the mother'sbladder to drain and collect the urine. A series of three diagnosticchallenges are administered, in each case followed by a six hourcollection of urine. In the first challenge 3 grams of calcium EDTA isgiven in 100 cc of NS over 30 minutes by intravenous piggyback. Theurine is collected over six (6) hours beginning with the administrationof the drug. A similar provocation is done using DMPS. A dosage of200-300 mg of DMPS is given via either an oral or intravenous routefollowed by a six (6) hour collection. Since the mother weighs 175 lbsand DMSA comes in 250 mg capsules, the mother is given 4×250=1000 mg ofDMSA orally, again followed by a six hour collection. These provocationsrevealed substantially elevated levels of lead, mercury, and cadmium.Each of these can cause birth defects in their own right. Each has asynergistic interaction with the others which greatly increases thetoxicity. The presence of these toxic metals explains the observed birthdefects.

Example 4 Maternal Chelation in the Lactating Female for the Benefit ofthe Suckling Newborn

Toxic heavy metals can be transferred to the neonate across thebreast-milk just as they are transferred across the placenta. To protectthe fetus from accumulating toxic metals an alternate route of excretionshould be provided. If some of the toxic metals in the blood areexcreted into the maternal gut or maternal urine then less is availableto be excreted via the breastmilk, and thus to the infant. Excretioninto the gut is favored by the presence of binding agents, including:activated charcoal, cilantro, chlorella, ETDA (which is minimallyabsorbed from the gut) and garlic or other herbs with the highsulfhydryl content. Also, increased bowel motility favors gut excretion.Any factor which increases bowel motility will favor excretion. VitaminC is useful in this regard.

Urinary excretion is favored by fluid administration, either orally orintravenously. Alkalinizing the blood favors excretion of metals fromtissue into the blood. Alkalinizing maternal urine may favor excretionof metals from the blood into the urine. Oral administration of antacidsallows acid to be excreted from the blood into the gut where it isneutralized. Thus, the mother is given oral EDTA, garlic, and activatedcharcoal as well as oral antacids. With these protections the toxinexcretion is favored and redistribution to unintended targets isminimized.

The mother could be treated first with a series of DMSA treatments,mobilizing lead into the urine. Only a small amount of DMSA is used andDMSA is readily excreted into the urine. This lowers the leadcontent—and since lead makes other metals more toxic, this will not onlyreduce the amount of lead reaching the fetus, but also reduce thetoxicity of any other metals reaching the fetus. The toxicity of DMSA isreduced by co-administration of zinc. Oral methionine can be used toprevent DMPS from crossing membranes. After several treatment cycleswith DMSA, DMPS is used to root out mercury, the second most toxic metalafter palladium.

The maternal chelation treatments can be done one day per week. Thechelating agents will generally be cleared from the maternal blood intwo to six (2-6) hours. The infant can consume stored milk during thistime period and after the chelating agent has passed into the maternalurine the infant can return to breastfeeding. One to two days later thematernal red blood cells can be checked for toxic metals. If thechelation therapy is successful then the red blood cells with bedepleted of toxic metals as these toxins were excreted into the urineand gut. Since the red blood cells are the source of heavy metals forthe infant, reduction in heavy metals in the maternal RBCs will suggestthat the chelation therapy is successful in protecting the infant fromheavy metal transfer.

Example 5 Maternal Chelation in Women with Multiple Previous SpontaneousAbortions

The patient is given a chelation-provoked urine test that diagnoses leadtoxicity. For the test, the woman is administered a protocol of oralDMSA 250 mg once by mouth three times a day, and her urine is collectedover a period of twenty-four (24) hours. The test results indicate thather body contained a store of lead.

After this diagnostic chelation, she is given a therapeutic chelationtreatment with three capsules of DMSA three times a day for three days aweek. Each three-day cycle constitutes one cycle of treatment, and thepatient typically receives fifteen (15) cycles of treatment. Asubsequent chelation-provoked urine test reveals a decrease in totalbody lead. The patient stops her chelation treatments and prepares toachieve pregnancy. She would be expected to achieve pregnancy and,subsequently, deliver a healthy baby at term.

Example 6 The First Time Mother Presenting with Spontaneous Abortion andVaginal Bleeding, and a Positive Pregnancy Test

A patient might present with vaginal bleeding, a positive pregnancytest, and a recent spontaneous abortion. The patient would be given adiagnostic oral provocation chelation. Oral provocation would be givenby DMSA 250 mg once by mouth three times a day. During the provocationher urine would be collected for 24 hours.

The diagnostic provocation would reveal a store of lead and tin in herbody. Subsequently, she would be given oral DMSA with fifteen cycles oftreatment. Having completed her DMSA treatment she is now ready toachieve pregnancy, but will continue chelation treatments because shewill not have removed all of the lead. She continues chelationtreatments in a manner which is coordinated with the menstrual cycle.She does this by beginning chelation in each cycle with the onset ofheavy or moderate bleeding, which would indicate the beginning of a newcycle. She continues the chelation treatments until she detects fertilemucous at her entroitus, indicating the onset of the fertile period.Alternatively, she could stop after eight (8) days of chelationtreatment. By either of these two methods she restricts her chelationtreatment to the early part of her cycle, when she is not fertile. She,subsequently, would became pregnant and not miscarry. She would also begiven oral EDTA as a chelation treatment during pregnancy. At theconclusion of the pregnancy, she would deliver a healthy child.

Example 7 The Mother Presenting with a Previous Child with AttentionDeficit Disorder

This patient would present with a previous child with attention deficitdisorder, behavioral problems, autism spectrum disorder and poorlanguage development. The mother-patient might be diagnosed as havingelevated levels of mercury using hair analysis or other suitablediagnostic methods. She would be given oral DMPS 300 mg once a week. Atthe conclusion of the pregnancy, her subsequent child would not haveattention deficit disorder.

Example 8 The Lactating Mother with High Lead and Mercury

This patient may have experienced three recurrent spontaneous abortions.She would be given an intravenous injection of DMPS as a diagnosticprovocation. Her diagnostic provocation would reveal that she had leadand mercury.

It is well known that lead and mercury are transferred to the infantthrough the breast milk. In order to prevent the lead and mercury fromtransferring into the breast milk, oral therapeutic chelation of themother would be performed by both oral EDTA and oral DMPS. The oralchelating agents being poorly absorbed in the human alimentary canal,tend to remain in the gut. As a result, lead and mercury are attractedto the gut and excreted in the feces and, therefore, less lead andmercury get transferred to the child through the breast milk.

Example 9 Gestational Chelation

In this case, a woman could be a 35-year-old gravida 4, para 3, whopresents with a history of three previous children with autism. She isnow pregnant with the fourth. She wonders if anything can be done toprevent autism in the fourth child. The first set of treatments involvesbinding the metal toxins in the gut. She is given oral EDTA, whichremains in the gut, and oral garlic. During chelation treatments, she isalso given activated charcoal oil orally, which binds the mobilizedtoxins in the gut. When she gets the chelation treatments, she alsotakes oral antacids to lower her systemic PH so that metal toxins arefreer to leave the cells. She is placed on a program of oral vitamin Cand oral selenium. The oral vitamin C augments her own natural abilityto make glutathione. She also takes L-Cysteine and N-Acetyl-Cysteinewhich also augment the natural ability to make glutathione. She takesoral selenium which binds the heavy metals and takes them out ofsolution by forming irreversible, tight heavy metal selenites which areunsoluble and effectively bind the heavy metals so that they cannot doany harm.

Chelation therapy preferably begins with the water soluble chelatingagent EDTA because EDTA does not cross membranes well. The urine, whichis collected after EDTA is analyzed for beneficial mineral nutrients,such as copper, zinc, manganese, et cetera, and chromium and whateverbeneficial nutrients have been removed by the EDTA are replaced orally.After the EDTA has been used to lower lead concentration, antibioticscan also be used as chelators.

Next, the patient is given oral DMSA with zinc. Oral DMSA with zincallows the oral DMSA to be used as a zinc chelator as it goes from thestomach to the blood stream bringing zinc into the body. Once in thebody, it picks up lead, mercury and other heavy metal toxins and isexcreted in the urine, thus this demonstrates the principle of boomerangchelation in which the chelating agent is used to bring in a nutrientbefore removing a toxin. As discussed above, the principles of boomerangchelation are that the patient is given a high oral concentration of anutrient mineral which is weakly chelated, along with the chelator. Dueto mass action, chelator transports the mineral across the gut into thebody. Once in the body, the chelator picks up a toxin for which it hasstronger affinity, this usually being something more toxic, such as leador mercury. This minimizes the harmful effects of the chelating agents.

Next, a DMPS may be used. DMPS has very high affinity for mercury, whichis the second most toxic metal. Since mercury is the second most toxicmetal, excretion of mercury is a high priority. Absorption of mercury byeither the brain or the fetus can be blocked by a concurrentadministration of methianine. Thus, a protein meal or oral methianineare used before DMPS and these then block the DMPS from getting intoeither the brain or the baby. Then the DMPS can be given orally and itcauses urinary excretion of the mercury.

Finally, lipoic acid can be used. Lipoic acid crosses membranes easilyand, therefore, a different principle is used with lipoic acid. There isa small amount of lipoic acid placed in the amniotic cavity. It will beabsorbed by the baby. Lipoic acid can then act as a chelator, startingin the baby's compartment and diffusing out into the maternalcompartment. Since the maternal compartment is much larger, there willbe a drop in the toxins within the baby, as these toxins getredistributed into the larger maternal compartment. This method ofchelation will work best if the mother is previously depleted of toxicmetals so that lipoic acid could not carry a toxin from baby into motherand then pick up another toxin in the mother and bring it back into thebaby. So this is why the preparation is done with water solublechelators which would not cross membranes. These would deplete the bloodvessels and the body of toxins, so that when chelators, such as lipoicacid is given, it will cause a net movement of toxins from the baby intothe mother because there are more open toxin binding sites since themother has been depleted of metal toxins.

In a pregnancy provocation, a number of things need to be demonstrated.The most important thing that needs to be demonstrated is that when thechelator is given, that there is not redistribution of toxins from themother into the baby. Thus, the three tests of monitoring are used. Oneis amniotic fluid; any metal; second is red blood cell heavy metals; andthird is maternal urine heavy metals and the fourth is maternal gutheavy metals. The goal of a successful chelation treatment would be todeplete the red cells of heavy metal toxins such that the toxins areeither excreted in the urine or excreted in the gut without significanttransfer to the baby. This can be facilitated by placing in the gut,nonabsorbable chelators, such as oral EDTA and oral garlic. Thepregnancy chelation is obtained in maternal urine, maternal feces,maternal red blood cells and amniotic fluid or fetal urine. Then, thechelatoring agent is given to the mother. This could be calcium EDTA,intravenous or oral DMPS or oral DMSA. If significant amounts of oralbinders are given, much of the mobilized metal toxins will become boundin the gut and excreted. If vigorous hydration is given either oral orintravenously, then what does not get bound in the gut will tend to beexcreted in the urine, since urine can constantly flow out of thematernal kidneys, whereas the fetal amniotic fluid is a closedcompartment. A very small catheter can be placed in the fetalcompartment by placing a small epidural or spinal needle into theamniotic cavity and then passing an epidural catheter through such aneedle Amniotic fluid then can be sampled before and after chelationtreatment to determine whether there is a movement of metal toxins frommother into baby after maternal chelation.

If there is no significant mobilization of metal toxins from mother intobaby during the diagnostic chelation, then the mother can besuccessfully depleted of heavy metal toxins while at the same timereplenished with beneficial mineral nutrients. Over time, the motherwill then become relatively clean of toxins comparted to what shestarted and compared to the baby. Most of the metal toxins bioconcentrate into the fetus at levels 200% to 800% of what they are inthe mother, so in general, the chelator which could mobilize toxinsacross the placenta should be likely to mobilize them in the directionfrom baby to mother, since toxins are concentrated in the baby relativeto the concentrations in the mother. After a period of EDTA chelationshave been given, the mother will be relatively depleted of lead andother heavy metal toxins. This can be followed by a period of treatmentwith oral DMSA combined with zinc. The oral DMSA with zinc will resultin boomerang chelation transporting zinc and lead out. Again, adiagnostic chelation needs to be done to verify that there is nosignificant transport of toxins from mother into baby.

Finally, DMPS can be used and again, a diagnostic chelation is done asdescribed above, to demonstrate that the DMPS does not mobilize toxinsfrom mother into baby. Separation with oral methianine is given to blocktransport of toxins into the baby. After the mother has been treatedwith one or more of the above chelators, the mother is relativelydepleted of metal toxins. During the normal course of pregnancy, toxinsbio-concentrate from the mother into the baby so the normal baby willhave higher concentration of toxins than the mother originally had inher system. Finally, lipoic acid is given. The maximum safety wouldresult from doing lipoic acid through the epidural catheter. This wouldmean that a small amount of lipoic acid is given in a small volume ofamniotic fluid and then picks up toxins there, diffuses across theplacenta and into the larger, much larger maternal volume ofdistribution so that there will net export of toxins from the baby intothe mother.

If it is relatively certain that the mother has been depleted of toxins,she can take oral lipoic acid which will also result in redistributionof toxins from the higher concentration found in the baby to lowerconcentration found in the mother.

Before provocation and after provocation monitoring of maternal redblood cell elements can also demonstrate a beneficial effect ofchelation. The heavy metal toxins that the baby is exposed to are thosecarried on maternal serum proteins and maternal blood cells, especiallythe red blood cells. Before and after chelation should demonstrate thatthe red blood cells are depleted of heavy metal toxins, and thus theamount of heavy metal toxins the baby is exposed to should be decreased.However, one has to recall that the red blood cells can either acceptheavy metal toxins from maternal tissues or baby tissues, or disseminateheavy metal toxins either through maternal tissues or from baby tissues.

Finally, methods of chelation treatments can be used in the mother whichmerely augment her normal processes. Specifically, this could be eitherhigh dose vitamin C, which would augment production of glutathione and,therefore, would cause excretion of heavy metals into the gut. If theseheavy metals are bound in the gut by chelators which are bound in thegut, then the natural chelation mechanism will work to deplete thematernal system and maternal red blood cells of heavy metal toxins.Thus, the baby will be exposed to less toxins. Another benefit ofglutathione is that glutathione is a detoxifier of many other metaltoxins, such as pesticides. Thus, the availability of glutathione willdetoxify many other toxins. Glutathione could be done in addition tointravenous vitamin C. Intravenous vitamin C also detoxifies not onlyheavy metal toxins, but many other toxins, including pesticides. Thus,either intravenous vitamin C or intravenous glutathione or both incombination would be a general detoxification treatment, which wouldcause elimination of heavy metal toxins, organic chemical and pesticidetoxins.

Actual Cases:

Case No. 1: The patient had multiple previous spontaneous abortions. Shereceived a chelation-provoked urine that was used to diagnose leadtoxicity. This was done by taking a protocol of oral DMSA 250 mg once bymouth three times a day. She collected her urine for 24 hours. Theresultant test indicated that her body contained a store of lead; onprovocation, her urinary lead concentration was 20 mcg/g creatinine.After this diagnostic chelation, she was given therapeutic chelationwith DMSA three capsules three times a day for three days a week. Eachthree-day cycle would constitute one cycle of treatment. This patientreceived 15 cycles of treatment which would be typical. A follow-upchelation-provoked urine revealed a decrease in total body lead. Shethen stopped her chelation and prepared to achieve pregnancy. Sheachieved pregnancy and, subsequently, delivered a healthy baby at term.

Case No. 2: The patient presented with vaginal bleeding and a positivepregnancy test. She had a spontaneous abortion and, subsequently, wastested by oral provocation. Oral chelation provocation was given by DMSA250 mg once by mouth three times a day. During the provocation her urinewas collected for 24 hours. The diagnostic provocation revealed a storeof lead and tin in her body; the urinary lead concentration afterprovocation was 14 mcg/g creatinine, and the tin was 9 mcg/g creatinine.Subsequently, she was given oral DMSA with five cycles of treatment.She, subsequently, became pregnant and did not miscarry. She was alsogiven oral EDTA during pregnancy. At the conclusion of the pregnancy shedelivered a healthy child.

Case No. 3: The patient had a previous child with attention deficitdisorder, behavioral problems, autism spectrum disorder and poorlanguage development. The patient was diagnosed as having mercury by theuse of a hair analysis; mercury was 1.5 mcg/g hair. She was given 500 mgof oral NAC per day throughout the pregnancy. The NAC promotes theformation of glutathionine, which is the body's natural chelating agent.She was also given vitamin C and selenium. At the conclusion of thepregnancy, her subsequent child did not have attention deficit disorder.

Case No. 4: The following illustrates the use of preconceptionalchelation as a treatment for infertility and also prevention ofmiscarriage. The patient was a 33-year-old G4P2022 who was infertilewith two previous miscarriages. She had a chelation provocation usingfour (4) capsules of DMSA 250 mg followed by a six (6) hour urinecollection. There was also an initial unprovoked urine collection. Theunprovoked lead was 0 mcg/g creatinine and the provoked lead of 13.6mcg/g creatinine. The unprovoked cadmium was 0.73 mcg/g creatinine andthe provoked cadmium was 1.79 mcg/g creatinine. The unprovoked tin 2.5mcg/g creatinine and the provoked was 12.5 mcg/g creatinine. The patientunderwent four (4) months of treatment with oral DMSA. She received four(4) capsules of DMSA (250 mg capsules) three (3) times daily and three(3) days per week followed by a four (4) day rest period. After the four(4) month treatment she had a follow up provocation. The lead was downto 1.34 mcg/g creatinine from previous level of 13.6 mcg/g creatinine.The cadmium was down to 0.18 mcg/g creatinine from previous 1.79 mcg/gcreatinine. The tin was 0.9 mcg/g creatinine down from previous 12.5mcg/g creatinine. During the treatment her energy level improved and herchronic fatigue resolved. She had a successful term pregnancy. This caseillustrates chelation to treat infertility and prevent miscarriage.

Case No. 5: The patient is a 27-year-old G0P0 with irregular menstrualcycles and chronic fatigue, but her chief complaint was infertility. ADMPS chelation provocation was performed which revealed (all values inmcg/g creatinine):

Lead  6.39 (normal <1.41) Antimomy  0.84 (normal <0.14) Mercury 38.55(normal <6.97)

She also had an EDTA provocation (in mcg/g creatinine):

Lead  25.14 (normal <1.41) Aluminum 176.8 (normal <98.7) Cadmium  3.18(normal <0.76) Nickel  36.9 (normal <9.5) Uranium  0.33 (normal <0.013)

She then had a laser laparoscopy for endometriosis and soon becamepregnant. She subsequently miscarried at fourteen (14) weeks. After themiscarriage, she had chelation treatments. This consisted of 3 grams ofcalcium EDTA and 3 grams of vitamin C intravenous push two (2) times perweek. She also had DMSA 500 mg per day orally. After a period of timeshe had repeat diagnostic provocations to determine readiness forpregnancy. On the repeat EDTA provocation her lead had previously beeneighteen times (18×) normal and now was down to eight times (8×) normal.The aluminum was previously two times (2×) normal, now down to twotenths of (0.2×) normal. The nickel was previously four times (4×)normal, now down to three (3×) normal. On the repeat DMPS provocationher lead was previously four times (4×) normal, now down to normal.Mercury was previously five times (5×) normal, now down to normal.Antimony was previously six times (6×) normal, now down to one and onehalf times (1.5×) normal. The patient's chronic fatigue improved. Shesubsequently achieved pregnancy and delivered a healthy baby at term.After the birth the baby was standing at two (2) months of age anddisplayed above average neurological development. This case illustratesprevention of miscarriage by chelation and exemplary neurologicdevelopment in a child whose mother was previously known to havemultiple neurotoxins.

Case No. 6: The patient came to labor and delivery after a relativelyuneventful pregnancy. After the patient came to labor and delivery, themother was placed on the fetal heart rate monitor. The monitor did notshow any evidence of decelerations that would be indicative of danger,however, the tracing also did not show any acceleration that would beindicative of safety. After several hours, the patient had a suddenbradycardia indicative of a sudden fetal distress in the baby. Sinceobstetric staff had been present in labor and delivery, an immediatecesarean section was performed with the baby delivered in sixteen (16)minutes, a very rapid response time. Despite the outstanding obstetricalcare given in this case, the infant suffered very severe brain damageand was finally taken off the respirator and allowed to die severalmonths after birth. Three days after delivery, the mother was given anoral DMSA diagnostic provocative chelation challenge. The results ofthis test, a chelation-provoked urine test, revealed the presence ofboth lead and mercury. Both lead and mercury impair the function of theKrebs' cycle which is the main power generating and energy generatingbiochemical mechanism of the cell. There were other vitamin deficienciesthat exacerbated the problems associated with lead and mercury. Inaddition, both lead and mercury generate free radicals. Much of thebrain damage that occurs during fetal distress, or for that matter withadult stroke or other ischemic scenarios, occurs after the event; thisis the mechanism of ischemia-reperfusion. In the ischemia-reperfusionperiod brain damage increases because of (1) energy failure, (2) freeradical stress and (3) glutamate release. Glutamate release is increasedbecause of the mercury that increased the presence of glutamate.Glutamate is the main excitotoxic neurotransmitter of the brain. Whenlarge amounts of glutamate are released, they overstimulate the alreadyenergy-depleted cells and cause further damage in a feed-forwardmechanism. Therefore, the presence of mercury increased the glutamateand caused increased brain damage. In addition, both lead and mercurycause the production of free radicals which increases tissue damage. Inaddition, both lead and mercury block pyruvate dehydrogenase. Thisenzyme is the gateway for energy stores, coming into the cell. Blockageof pyruvate dehydrogenase results in severe compromise of the cell'senergy producing capacity.

The use of the chelation-provoked urine test in this case demonstratesthat the causes of the fetal impairment, specifically, lead and mercury,which have nothing to do with obstetric care. This may be beneficial inmalpractice litigation to prevent unfair blaming of the physician when,in fact, another cause (namely, lead and mercury) may actually the causeof the brain damage. In this case, the plaintiff's attorney settled fora nominal amount ($50,000) when he realized he could not suppress theresults of the chelation provoked urine test or exclude it from thecase. Accordingly, it is within the scope of the present invention toprepare a report on the test results and introduce the results of thechelation diagnostic tests in such a malpractice case.

Case No. 7: Similar to Case No. 6 presented above, the patient came tolabor and delivery with a relatively normal tracing and even hadnumerous accelerations. There was the sudden reduction in the fetalheart rate, known as a bradycardia. This was a sign of fetal distress.Because obstetricians were standing by, the baby was delivered in 12minutes, a remarkably rapid response time. Despite the rapid response,the baby still suffered hypoxic ischemic encephalopathy that resultedfrom fetal distress. This patient had oral provocative DMSA challengeswith one 250-mg capsule of DMSA followed by a six (6) hour urinecollection. The results of this provocation are as follows (all valuesin mcg/g creatinine):

lead  4.79 (normal <1.41) nickel 77 (normal <9.5) tungsten  6.41 (normal<0.34) uranium  0.05 (normal <0.031)

The patient also had a DMPS provocation. The challenge was one 300-mgcapsule of DMPS followed by a six (6) hour urine collection. The resultswere as follows:

lead  4.6 (normal <1.41) nickel 132 (normal <9.5) tungsten  7.07 (normal<0.34) uranium  0.034 (normal <0.013)

These provocations reveal the presence of toxic metals, which couldexonerate the physician in the event of a lawsuit, or even betterdiscourage the plaintiffs' attorney from filing a lawsuit. No lawsuitwas filed in this case.

Case No. 8: In another case, a mother was known to have lead and mercurybecause she had diagnostic provocation before pregnancy. She was givenoral EDTA 3000 mg per day, vitamin C 5000 mg per day, selenium 200micrograms three (3) times per day, and garlic 6000 mg per day. At thetime of delivery, she had a normal delivery with no evidence of fetaldistress. In this case, oral EDTA limited the fetal exposure to maternallead which is usually substantial in pregnancies. This fetus was enabledto have a normal pregnancy and delivery because of the oral chelationtreatment. Subsequent to the delivery, the child was healthy andneurologically normal.

Case No. 9: The patient was a 23-year-old G-4, P-3003 who had beenadmitted with pain secondary to preterm labor. The gestational age was27 weeks by early ultrasound, but 24 weeks by fetal size. The patienthad intermittent variable fetal heart rate decelerations. The initialimpression was intrauterine growth retardation with preterm labor. Dueto recurrent decelerations and severe preeclampsia, the decision wasmade to proceed with caesarian section. Apgar test scores were 3 at 1minute, 3 at 5 minutes, 3 at 10 minutes with a birth weight of 631grams. These Apgar test scores indicate severe hypoxic injury to thenewborn.

In the postpartum period, the mother was examined with urine organicacid test. This revealed deficiencies of vitamin B1, B2, B3 and vitaminC. Marked deficiencies were seen of folic acid and B12. An unprovokedassessment of urine toxic metals revealed elevated amounts of tin anduranium, as well as the presence of mercury, antimony and cadmium atapproximately the level of the reference range. Provocation with EDTA (3grams calcium EDTA in 100 cc NS over 30 minutes followed by a 6 hoururine collection which begins with the infusion of the calcium EDTA)lead to significant excretion of lead, mercury, cadmium and uranium. Theuranium was more than forty times (40×) the reference range. Provocationwith DMSA (1000 mg PO×1 followed by 6 hour urine collection) resulted inexcretion of a number of metals, including lead, mercury, cadmium anduranium. Uranium appeared at a level at more than one hundred times(100×) the reference range.

The findings here provide an example of a peripartum tragedy caused byseverely elevated levels of maternal heavy metals and deficiencies infolic acid and vitamin B12. The clinical findings in this case couldhave been influenced and therefore explained by the previouslyunsuspected presence of toxic metals. These toxic metals have numeroustoxic effects, including impairment of the Kreb's cycle, which leads toimpaired energy production by the fetus, and thereby contributes tofetal distress. Preconception evaluation of toxic maternal metal levels,vitamin deficiencies and appropriate therapy, including chelationtreatment and vitamin supplementation, will avert such complications.

Case No. 10: The patient was a 34-year-old G-3, P-2 at 36 4/7 weeks. Thepatient had decreased fetal movements for fifteen (15) days withcontractions every fifteen (15) minutes. The patient came in with anonreactive Non-Stress Test (NST) and decreased fetal movements. Pastmedical history was unremarkable. Pelvic exam revealed a minimallydilated cervix (1 cm dilated, 70% effaced, −2 station).

Fetal evaluation revealed that the health of fetus was in jeopardy. Thepatient was admitted to the hospital with nonreactive fetal heart ratetracing and minimal variability. Acoustic stimulation was performed andthe fetus was unresponsive. The fetus had a period of late decelerationsand a positive contraction stress test.

The patient was taken for a primary cesarean section. The initialassessment of the neonate suggested hypoxic depression. The Apgar testscores were 0 at 1 minute, 4 at 5 minutes, 8 at 10 minutes. Therespiratory evaluation of the neonate (cord gas) revealed respiratoryacidosis (pH 7.16, PCO2 51, PO2 59, bicarb 17, base excess −11). Theneonate was found to have hyperphosphatemia, hypomagnesemia,hyperkalemia and constriction of the ductus arteriosis. The mother wasalso found to have elevated nucleated red blood cells to 130, suggestinglong-standing hypoxia with bone marrow response. In summary, theclinical scenario describes a severely sick neonate.

Biochemical evaluation by gas-liquid-chromatography indicated thefollowing:

-   -   Chlorinated pesticide evaluation revealed DDT and DDE.    -   Organophophorus pesticides were negative.    -   Urine organic acid evaluation revealed deficiencies of thiamine,        riboflavin, niacin, B12, biotin, folate, manganese, copper,        magnesium, vitamin C and lipoic acid,    -   There was disruption of fatty acid oxidation, markedly elevated        lactate and pyruvate, with decreases in the other Kreb's cycle        intermediates, suggesting that energy metabolites were blocked        from entering the Kreb's cycle at pyruvate dehydrogenase.    -   Evaluation of urine amino acids suggested deficiencies of folate        and molybdenum.

Urinary heavy metal testing was as follows: unprovoked urine revealedelevations of lead, mercury, aluminum, antimony, arsenic, barium,gallium, nickel, tin, tungsten and uranium. DMSA challenge (250 mg PO×1followed by 6 hour urine collection) revealed elevated amounts of lead,aluminum, antimony, barium, nickel, gallium, tin, tungsten, and uranium.DMPS provocation was done with DMPS 300 mg PO×1 followed a 6 hour urinecollection. DMPS provocation revealed elevated levels of lead, mercury,aluminum, antimony, cadmium, nickel, tin, tungsten and uranium. Insummary, there were numerous biochemical factors which would harmfullyinfluence the baby's energy metabolism. These factors, includingnutrient deficiencies and toxic metals, could explain the unfortunatebirth outcome.

Case No. 11: The patient was a 26-year-old G-5, P-3013 who had come tothe hospital with severe abdominal pain for five (5) hours and bleeding.The baby had bradycardia (slow heart beat) with a heart rate 70-80 bpm.The mother was taken for an emergency Cesarean section. The neonate wasborn in very poor condition—the Apgar test scores were 0 at 1 minute, 0at 5 minutes, 2 at 10 and 4 at 20 minutes. A blot clot covering 60% ofthe placenta indicated abruption.

Urine organic acid analysis revealed deficiencies of B12, riboflavin,vitamin C, and copper. A DMSA provocation was performed by giving 1000mg DMSA orally×1 followed by six (6) hour urine collection. DMSAprovocation revealed elevated levels of lead, mercury, tin, uranium andtungsten.

An EDTA provocation was performed by intravenously infusing 3 grams ofcalcium EDTA in 100 cc normal saline over thirty (30) minutes, followedby a six (6) hour urine collection. Results revealed elevated levels oflead, mercury, aluminum, cadmium, gadolinium, gallium, tin, tungsten,and uranium.

This case portrays an alarming scenario in the field of obstetrics. Anunknown patient appears at the hospital requiring an emergent Cesareansection, and despite the best efforts of the obstetrician, disasterresults. To defend against malpractice litigation, the obstetrician mustdemonstrate the results were due to a cause other than the treatmentprovided at the hospital.

In this case, multiple heavy metals were present, as well as nutrientdeficiencies. These biochemical factors can explain the poor birthoutcome. This gives the obstetrician a defense against an unfairmalpractice suit.

Case No. 12: The patient was a 17-year-old G1 P0 at 39 weeks gestationalage who presented to the hospital with labor pains. The fetal heart ratetracing revealed worrisome decelerations. Meconium was noted at the timeof the delivery. The baby was floppy at birth and had no respirations(Apgar test scores 3 at 1 minute and 6 at 5 minutes). The neonatologistwas called to revive the depressed baby. The infant had a poor responseto resuscitation. The cord gas evaluation revealed the baby who wasacidotic (pH 7.03). The pCO2 was 73 indicating respiratory acidosis.Base excess was −13, indicating metabolic acidosis.

Urine organic acid analysis revealed impaired fatty acid oxidation anddeficiencies of carnitine and/or riboflavin. Pyruvate and lactate wereboth elevated, suggesting impairment of the Kreb's cycle. Urine organicacid assessment indicated deficiencies of vitamin C, vitamin E, vitaminsB1, B2, B3, B5, B12, biotin, co-enzyme Q10, carnitine, lipoic acid,magnesium, selenium, manganese, cromium, argentine, and Vanadium.

A DMPS provocation was performed by giving DMPS 300 mg PO×2 followed bya six (6) hour urine collection. Urine element testing revealed markedelevation of nickel as well as abnormally elevation of arsenic, cadmiumand lead.

In summary, it is generally thought, in obstetrics, that fetal distress,low Apgar test scores, acidotic cord pH have little do to with cerebralpalsy and other neurologic untoward outcomes. This is based on a largequantity of establish science that remain unpersuasive in the courtroom. It is unpersuasive because the obstetrician is unable to point toan alternative cause for the bad outcome. In this case we see elevationof nickel which toxically impairs the electron transport chain. Cyanide,another electon transport chain toxin, causes biochemical asphyxiationin the presence of normal amounts of oxygen by blocking the beneficialeffect of oxygen on the electron transport chain. Lead, cadmium andarsenic can impair the function of pyruvate dehydrogenase. This enzymeis critical to the function of the Kreb's cycle, and its impairment isindicated by the elevation of pyruvate and lactate. The variousdysfunctions of the Kreb's cycle and electron transport chain couldimpair the baby's energy production, i.e. they are not caused by anynegligence by the obstetrician, and there is currently no technology inobstetrics that can detect these problems. Thus, the obstetrician candemonstrate that the problems in the baby were not caused by him.

Case No. 13: The patient was a 31-year-old Latin American female G1P0.She presented with a chief complaint of infertility. An EDTA provocationwas performed on the woman and her husband. This was done with 3 gramsof EDTA and 3 grams of vitamin C intravenous push followed by a six (6)hour collection. Lead was 6.15 mcg/g creatinine (normal <1.41); mercury3.09 mcg/g creatinine (normal <6.97); cadmium was 0.86 mcg/g creatinine(normal <0.76). The husband's test results were similar.

The woman received ten (10) intravenous EDTA chelations as did thewoman's husband. The chelation treatments for both the husband and thewife were done by giving 3 grams of calcium EDTA plus 3 grams of vitaminC intravenous slow push once per week. She delivered a normal healthybaby at term. This child has a large vocabulary relative to his age of 2years old and seems to have admirable neurological development.

Case No. 14: The patient was a 32-year-old white female, gravida 2, para2003 who became pregnant after having been successfully treated by aninfertility doctor for an ovulatory disorder following a previouspregnancy. She was initially found to have mercury on a hair test andwas treated at pregnancy with selenium. She had a second pregnancy anddelivered a second healthy infant before having her metals evaluated.

In October of 2003, after the first two pregnancies, the patient had aDMPS provocation which revealed the following results (all values inmcg/g creatinine):

lead  7.9 (normal <1.41) mercury  7.3 (normal <2.14) antimony  0.48(normal <0.14) arsenic 159 (normal <50) cadmium  0.82 (normal <0.64)nickel  9.3 (normal <9.5) thorium  0 (normal <0.124) tin  10.4 (normal<2.04) uranium  0.042 (normal <0.026)

The patient was treated preconceptually. She had a series of intravenousDMPS chelation treatments from October 2003 to May 2004. After thesechelation treatments, the lead was reduced to 0.9 mcg/g creatinine, themercury to 6 mcg/g creatinine, the antimony down to 0.05 mcg/gcreatinine, arsenic of 20 mcg/g creatinine, cadmium of 0.16 mcg/gcreatinine, nickel of 3.2 mcg/g creatinine, thorium of 0.019 mcg/gcreatinine, tin of 0.4 mcg/g creatinine, and uranium of 0 mcg/gcreatinine. She was given oral DMSA and essential daily defense and hada follow up in October 2005 when the lead was 2.6 mcg/g creatinine, themercury was 4.6 mcg/g creatinine, antimony was 0.18 mcg/g creatinine,arsenic was 34 mcg/g creatinine, cadmium 0.17 mcg/g creatinine, nickel0.7 mcg/g creatinine, thorium 0 mcg/g creatinine, tin 3.03 mcg/gcreatinine, and uranium 3 mcg/g creatinine. This experiment wouldsuggest that the therapeutic benefit was preserved because most of thechelation treatments were over by May 2004 and only a little bit ofchelation treatments occurred between May 2004 and October 2005.

During the treatment period, the patient had an intravenous EDTAprovocation in January 2004 which revealed a lead of 4.6 mcg/gcreatinine, mercury of 0 mcg/g creatinine, antimony of 0.18 mcg/gcreatinine, arsenic of 90 mcg/g creatinine, cadmium of 1.59 mcg/gcreatinine, nickel 41 mcg/g creatinine, thorium of 0.22 mcg/gcreatinine, tin 0.6 mcg/g creatinine. After intravenous EDTA and DMPSchelation treatments, in June 2004, she had lead of 5.5 mcg/gcreatinine, mercury 0 mcg/g creatinine, antimony reduced to 0.15 mcg/gcreatinine, arsenic reduced to 32 mcg/g creatinine, cadmium was 1.75mcg/g creatinine, nickel was 30 mcg/g creatinine, thorium 0.06 mcg/gcreatinine, tin 0.3 mcg/g creatinine. A little bit of DMSA withessential daily defense and the long-term follow up in October of 2005,was lead of 7.97 mcg/g creatinine, mercury of 9.4 mcg/g creatinine,antimony 0.09 mcg/g creatinine, arsenic 46 mcg/g creatinine, cadmium2.66 mcg/g creatinine, nickel 26 mcg/g creatinine, thorium 0 mcg/gcreatinine, tin 0.4 mcg/g creatinine, and uranium 0.012 mcg/gcreatinine.

This case demonstrates the benefit of preconceptual chelationprovocation and chelation treatments, and that the benefit can berelatively stable after a thorough series of chelation treatments.

Accordingly, the present invention can prevent birth defects,spontaneous abortions and childhood mental disorders and improve mentaldevelopment of the fetus, infant and child. Another aspect of thisinvention is that the person who benefits from the treatment, the child,is different from the person who received the treatment, the mother.Another advantage is that the processes of embryonic and fetaldevelopment and infant development, are re-imagined not as inexorablesequences that may result in disaster, but rather physiologic processesthat can be remedied when they go awry.

Organ and tissue development occurs as a timed sequence. It only occursonce. If development goes awry, the development cannot be repeated orrevised later. Reproductive chelation therapies, including chelationprovocation and chelation treatments, enhance the development of theorgans and tissues, including the brain.

The new reproductive chelation therapies discussed herein, includingchelation provocation and chelation treatments, can diagnose and removemetal toxins preconceptually, i.e. before the pregnancy has even beenconceived. This will reduce birth defects, miscarriages, and neuraldevelopmental problems without jeopardizing the fetus and/or embryo.

Reproductive chelation treatments can remove metal toxins duringpregnancy preventing or limiting the accumulation of toxic metals duringbrain growth and development. Reproductive chelation evaluations canidentify non-obstetric causes of fetal maldevelopment. This fetaldiagnostic information can demonstrate that fetal neural developmentalcatastrophes such as fetal distress and resultant brain damage can becaused by factors unrelated to labor management. This would be helpfulin malpractice litigation.

Reproductive chelation therapies can enhance development of the fetusand embryo with resultant better long-terms health. This can improve theintelligence of postnatal children and improve their long-termintellectual capacity, emotional development, psychological developmentand job performance.

Reproductive chelation therapies can improve neurologic developmentleading to improved postnatal function and better long-termintellectual, behavioral and emotional performance.

Reproductive chelation treatments can remove metal toxins from theoffspring so as to allow subsequent healthy development after treatmentis over.

Reproductive chelation treatments can be coupled with adjunctivemeasures, such as co-administration of mineral supplements, so as toprevent the harmful effects of chelation.

Neurological conditions contemplated for treatment by the inventioninclude but are not limited to attention deficit disorder (ADD), autism,dyslexia, and those described infra.

Structural disorders contemplated as amenable to the treatmentsdescribed herein include malformed organs, omphalocele, cysticdysplastic kidney, Potter's syndrome, urinary obstruction, bladderoutlet obstruction, atrial and ventricular septal defect, hypoplasticheart, AV canal, transposition of the great arteries, and coarctation ofthe aorta.

Brain and skull defects contemplated as amenable to the disclosedinvention include anencephaly, spina bifida, porencephalic cyst,holoprosencephaly, and certain forms of hydrocephalus.

As various modifications could be made to the exemplary embodiments, asdescribed above without departing from the scope of the invention, it isintended that all matter contained in the foregoing description shall beinterpreted as illustrative, being exemplary in nature rather thanlimiting. For example, the chelation therapies described above may alsobe used to diagnose metal toxins in men and detoxify these men prior totheir impregnation of their respective partners. Thus, the breadth andscope of the present invention should not be limited by any of theabove-described exemplary embodiments, but should be defined only inaccordance with the following claims appended hereto and theirequivalents.

What is claimed is:
 1. A method of determining a cause of a fetaldistress comprising: delivering an infant from a human female;administering chelating agents to the human female following deliveringthe infant, wherein administering the chelating agents to serve as aprovocative challenge; collecting a specimen from the human femalefollowing administering chelating agents wherein the chelating agentshave removed by chelation of heavy metals from the body of the humanfemale to the specimen of the human female; analyzing the specimen for apresence of heavy metals; and correlating said presence of heavy metalswith fetal distress.
 2. The method of claim 1 further comprising thesteps of calculating a suitable dosage of a chelating agent andadministering the dosage of the chelating agent to the human femaleprior to or during a subsequent pregnancy, thereby reducing likelihoodof a subsequent fetal distress.
 3. The method of claim 1 furthercomprising the step of preparing a fetal distress report based on theanalyzing and correlating steps.
 4. The method of claim 3 furthercomprising the step introducing the results of the chelation diagnostictests in a malpractice case.
 5. The method of claim 2 further comprisingthe step of when the human is a fertile female attempting to achievepregnancy and having a menstrual cycle with a fertile period and aninfertile period and then administering step is restricted to theinfertile period of the menstrual cycle.
 6. The method of claim 2further comprising the step of when the human is a fertile female who ispregnant then the calculating step comprises performing a calculationbased on the gestational age of the fetus of the pregnant human female.7. The method of claim 1 wherein the chelating agent is selected fromthe group of synthetic chelating agents consisting of BAL, DMSA, DMPS,CDTA, DTPA, DPA, NAC, TIRON, DFO, and TRIEN.
 8. The method of claim 1further comprising the step of co-administering the chelating agent withmineral supplements.
 9. The method of claim 2 further comprising thestep of co-administering the chelating agent with mineral supplements.10. The method of claim 1 wherein the chelating agent is engineered tohave a specific binding coefficient and a specificity for particularmetals.
 11. The method of claim 1 wherein the chelating agent isexcretable.
 12. The method of claim 1 wherein the levels of heavy metalidentified are subclinical.
 13. The method of claim 2 further comprisingthe step of repeating the administration of the dosage of the chelatingagent on a fixed schedule.
 14. The method of claim 1 wherein theadministration of the chelating agent is during lactation.
 15. A methodof determining a cause of a fetal distress comprising: delivering aninfant from a human female; administering chelating agents to the humanfemale following delivering the infant, wherein administering thechelating agents serve as a provocative challenge; collecting a specimenfrom the human female following administering chelating agents whereinthe chelating agents have removed by chelation of heavy metals from thebody of the human female to the specimen of the human female; analyzingthe specimen for a presence of heavy metals; correlating said presenceof heavy metals with said fetal distress; calculating a suitable dosageof a chelating agent; and administering the dosage of the chelatingagent to the human female prior to or during a subsequent pregnancy,thereby reducing likelihood of a subsequent fetal distress.